Muscle oxygenation and fascicle length during passive muscle stretching in ballet-trained subjects.

Muscle stretching transiently decreases muscle-blood flow corresponding to a muscle extension. It may disturb a balance between muscular oxygen demand and oxygen supply to muscles and reduce muscle oxygenation. However, muscle-stretching training may improve blood circulatory condition, resulting in the maintained muscle oxygenation during muscle stretching. The aim of this study was to investigate changes in muscle-blood volume (tHb) and tissue oxygenation index (TOI) during muscle stretching determined by using near-infrared spectroscopy (NIRS) in ballet-trained (BT) and untrained (C) subjects. 11 BT women who regularly perform muscle stretching and 11 C women participated in this study. Fascicle lengths, tHb and TOI in the tibialis anterior muscle were measured during passive plantar flexion from ankle joint angles of 120° (baseline) to 140°, 160°, the maximal comfortable position without pain (CP), and the maximal position (MP). At 160°, the % fascicle-length change from baseline was significantly lower in the BT than the C group, however, for the changes in tHb and TOI the significant interaction effect between the 2 groups was not detected. On the other hand, although the increases in the fascicle length from baseline to CP and MP were greater in BT than C, the tHb and TOI reductions were comparable between groups. We concluded that it appears that BT can extend their muscles without excessive reduction in muscle-blood volume and muscle oxygenation at relatively same but absolutely greater muscle-stretching levels than C. The attenuation in these indices during high-level muscle stretching may be associated with the repetitive muscle stretching of long-term ballet training.

Predominant synthesis of 5-hydroxyeicosatetraenoic acid by a cloned mastocytoma P-815 line, 2-E-6 cells.

Since mouse mast tumor P-815 cells produce the slow reacting substance of anaphylaxis, their 5-lipoxygenase activity was examined by determining the conversion of arachidonic acid to 5-hydroxyeicosatetraenoic acid (HETE). Mast tumor cells from mouse ascites fluid synthesized 12-HETE as a major and 5-HETE as a minor metabolite. Once the cells were transferred to an in vitro culture system, the predominant synthesis of 12-HETE was abolished and synthesis of 5-HETE was greater than that of 12-HETE. 2-E-6 cells, obtained by cloning the tumor cells, synthesized a negligible amount of 12-HETE, but produced a large amount of 5-HETE. When the 2-E-6 cells were inoculated into mice and harvested again from the ascites fluid, their ratio of 5-HETE to 12-HETE synthesis was similar to that of normal mouse peritoneal cells; that is, 12-HETE synthesis was much greater than 5-HETE synthesis. It is concluded that the predominant synthesis of 12-HETE in mast tumor cells was derived from natural peritoneal cells, which have very high 12-lipoxygenase activity. The cloned mastocytoma, 2-E-6 cells, should be useful in investigating regulation of 5-lipoxygenase activity.

Preventive effects of pyrroloquinoline quinone on formation of cataract and decline of lenticular and hepatic glutathione of developing chick embryo after glucocorticoid treatment.

When 0.25 mumol of hydrocortisone succinate sodium (HC) was administered to 15-day-old fertile eggs, almost all lenses of chick embryos treated with HC for 48 hr were classified as cataract stage IV-V (95%). A triple application of potassium pyrroloquinoline quinone (PQQ) (1.25 mumol/egg) at 3, 10 and 20 hr after HC treatment showed a preventive effect against the HC-induced cataract formation (I:45%, II:25%, III: 30%). PQQ also prevented the decline of GSH in the lens caused by HC. The decline of GSH in liver 24 hr after HC administration was prevented by PQQ. These data indicate that PQQ can modify HC-induced effects and that the preventive effect of PQQ against HC-induced decline of hepatic GSH seemed to influence HC-induced events in lens.

The hen's fertile egg screening test (HEST): a comparison between the acute toxicity for chick embryos and rodents of 20 drugs.

The possibilities of using developing chick embryos for evaluating drug activities and toxicities were studied by determining LD50 values for 20 drugs with 14 different pharmacological activities. Fifteen-day old chick embryos received drugs through the air cell and deaths were measured at 48 hr after the treatments. The LD50 values were determined and compared to the i.v., i.p., s.c. and p.o. values from mice listed in the Registry of Toxic Effects of Chemical Substance. The systemic toxicity of 15-day-old chick embryos to drugs were similar to those of mice with the following exceptions. The chick embryos seemed to be more sensitive than mice to antineoplastic or antibiotic agents such as actinomycin D and doxorubicin, whereas, LD50 values of cholinergic and cholinergic blocking drugs by this method were 10 to 20 fold of LD50 (i.v.) of mice. These observations are important for applying the hen's fertile screening test (HEST) to the determination of drug activities other than that of embryo toxicity or teratogenic activity.

Enhancement of 5-lipoxygenase activity in mastocytoma P-815 cells by n-butyrate treatment.

Cloned mastocytoma P-815, 2-E-6 cells were used to investigate regulation of 5-lipoxygenase activity. 2-E-6 cells had high 5-lipoxygenase activity with slight 12-lipoxygenase activity. The 5-lipoxygenase activity was increased over 5-fold by treatment of the cells with 1 mM n-butyrate for 18 h. the most effective dose range being 0.1-5.0 mM. Treatment with n-butyrate for 18 h was more effective than treatment for 40 h. Addition of n-butyrate to an untreated cell homogenate had no stimulatory effect. The enhancement of 5-lipoxygenase activity by n-butyrate was accompanied by new synthesis of protein(s). 12-Lipoxygenase activity was not increased so much as 5-lipoxygenase activity by the treatment. This is the first report of stimulation of 5-lipoxygenase activity in cultured cells. The different responses of the two lipoxygenases to n-butyrate treatment strongly suggest that 5-lipoxygenase is a different enzyme from 12-lipoxygenase.